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At least 919 records · Page 51Linked to original sources
PubMed2000

Effects on dogs of surface-induced hypothermia and rewarming on the right heart function and pulmonary circulation.

Hypothermia is commonly found in accidents on land and at sea, yet its pulmonary circulatory effects have not been studied before. To study the effects of hypothermia on the right heart function and pulmonary circulation, cardiac catheterization was carried out on nine anaesthetized beagle dogs. The dogs were cooled between ice bags until the temperature in the pulmonary artery was 25 degrees C and then rewarmed using a heating box especially constructed for this purpose. Heart rate decreased significantly (P < 0.01) during cooling. Cardiac output also diminished mainly because of decreased heart rate. Total pulmonary resistance increased in the cold (P < 0.05) and returned to the initial level during rewarming. The peak rate of increase in pressure (dP/dtmax) of the right ventricular pressure curve did not show any significant change. Retardation in relaxation in hypothermia was indicated by an increase (P < 0.01) in the peak negative dP/dt of the right ventricular pressure curve. According to our results, the contraction rate did not change, but the relaxation rate decreased significantly during cooling. No signs of heart failure were observed and all parameters returned to normal during rewarming. In conclusion, right ventricular function was not compromised even during deep hypothermia.

Animals↗
PubMed2006

Inhibition of cyclooxygenase-2 improves cardiac function following long-term preservation.

BACKGROUND: Cyclooxygenase (COX) is an intracellular enzyme that converts arachidonic acid to prostaglandin endoperoxide (PGG(2)). There are two isoforms of COX, namely constitutive COX-1 and inducible COX-2. It has been reported that COX-2 plays an important role in ischemia-reperfusion injury and that COX-2 mRNA and protein expression were up-regulated during cardiac allograft rejection. FK3311 is a suppressor of COX-2 activation. The purpose of this study was to evaluate the effectiveness of inhibiting COX-2 with FK3311 for the minimization of ischemia-reperfusion injury and for the improvement of donor heart function following transplantation in a canine model. MATERIALS AND METHODS: Adult mongrel dogs were used. After the measurement of hemodynamic parameters [cardiac output (CO), left ventricular pressure (LVP), and the maximum rates of increase and decrease in LVP (+/-LVdp/dt)], coronary vascular beds were washed out with a hypothermic (4 degrees C) University of Wisconsin (UW) solution following cardiac arrest in response to cold (4 degrees C) glucose-insulin-potassium solution. The heart was then excised and preserved in hypothermic (4 degrees C) UW solution for 12 h. FK3311 (3 mg/kg) was administered intravenously to five dogs prior to reperfusion, while vehicle was administered intravenously to a control group (n = 5). After 3 h of orthotopic transplantation using cardiopulmonary bypass, the hemodynamic parameters were compared with preoperative values of the donor animals under the condition of 10 mm Hg right atrial pressure and 5 mug/kg/min dopamine support. RESULTS: The recovery rates of CO and +/-LVdP/dt were significantly (P < 0.05) higher in the FK-treated dogs than in the controls (CO: 93 +/- 6 versus 66% +/- 4%; +LVdp/dt: 125 +/- 8 versus 77 +/- 10%; and -LVdp/dt: 81 +/- 7 versus 52 +/- 6%; for FK-treated versus control dogs, respectively). The recovery rate of LVP was higher in the FK-treated dogs than in the controls (90 +/- 5 versus 72 +/- 5%), but this difference was not statistically significant. Immunohistochemical staining revealed that COX-2 expression was reduced significantly in the myocardium of FK-treated dogs compared with controls. CONCLUSION: Hemodynamic parameters following transplantation were improved significantly in dogs treated with FK3311. Therefore, the inhibition of COX-2 improves transplanted cardiac function following long-term preservation.

Adenosine↗
PubMedDate not supplied

Effect of verapamil on left ventricular function at rest and during exercise in normal men.

Verapamil is a calcium channel blocking agent used primarily for treatment of arrhythmias and coronary artery disease. It may also depress myocardial contractility. The purpose of this study was to assess the effect of verapamil on left ventricular function. Twelve normal men, 22-29 years of age, were studied at rest and during exercise, with and without verapamil, using first-pass radionuclide angiocardiography. Verapamil was administered by continuous intravenous infusion to produce steady-state blood levels of 106-123 ng/ml. The heart rate, ejection fraction, stroke volume index, and end-diastolic volume index were measured with and without the drug. Verapamil increased the mean resting heart rate from 74 to 78 beats/min (p = 0.001), decreased the mean stroke volume index from 48 to 42 ml/m2 (p = 0.01), and decreased the mean end-diastolic volume index from 77 to 71 ml/m2 (p less than 0.05). No changes in cardiac index, ejection fraction, end-systolic volume index, or peak systolic pressure/end-systolic volume ratio were observed at rest. No differences occurred in exercise hemodynamics. Thus verapamil at therapeutic dose levels did not significantly depress contractility or have other clinically important hemodynamic effects at rest or during exercise in normal subjects.

Adult↗
PubMed1975

A direct comparison between internally and externally measured left ventricular systolic time intervals.

In 38 cardiac patients a direct comparison was made of systolic time intervals derived from the external carotid pulse tracing and from the central aortic pressure curve, simultaneously recorded by means of a catheter-tip micromanometer. In addition the transmission time of the upstroke and the incisura of the central pulse wave to the carotid artery was studied. In spite of close linear correlations, significant differences in absolute values were observed between internally and externally measured systolic time intervals. The transmission times of upstroke and incisura of the pulse wave also differed significantly. Both findings were directly related and dependent upon the heart rate.

Adult↗
PubMed1990

Invasive evaluation of left ventricular diastolic performance.

Diastole can be divided into four phases: 1. isovolumic relaxation; 2. early filling; 3. diastasis; and 4. atrial systole. The amount of left ventricular (LV) filling that occurs during each of these phases depends on: 1. myocardial relaxation; 2. the passive characteristics of the LV; 3. the characteristics of the left atrium, pulmonary veins and mitral valve; and 4. the heart rate. When diastolic function is normal, the net effect of these factors results in LV filling sufficient to produce an adequate cardiac output, while mean pulmonary venous pressure is maintained below 12 mm Hg. Diastolic dysfunction is normally manifest as pulmonary congestion. In the absence of systolic dysfunction, abnormal diastolic performance is usually due to abnormal relaxation and/or changes in the passive LV characteristics, external compression or disease of the mitral valve and left atrium. Invasive studies can quantify the rate of myocardial relaxation from the time course of the fall of LV pressure during isovolumic relaxation and the passive LV properties from the LV diastolic pressure-volume relation. In addition, frame-by-frame analysis of contrast ventriculography and conductance determination of LV volume can quantify the pattern of LV diastolic filling. Normally, at rest, most LV filling occurs early in diastole. Conditions that produce diastolic dysfunction, such as LV hypertrophy and ischemia, are associated with reduced early diastolic filling and an augmented importance of atrial systole. It is important to recognize that such patterns can occur in patients without clinically apparent diastolic dysfunction and in normals if left atrial pressure is sufficiently elevated. Furthermore, a normal pattern can occur in patients with severe diastolic dysfunction. Reduced early diastolic filling in the absence of pulmonary congestion indicates the loss of diastolic reserve, since the left atrium is being used as a booster-pump. This pattern of diastolic filling in a patient with symptoms of pulmonary congestion suggests diastolic dysfunction, even if systolic LV performance is normal.

Atrial Function↗
PubMed2002

Cardiopulmonary exercise parameters in children with atrial septal defect and increased pulmonary blood flow: short-term effects of defect closure.

UNLABELLED: Markedly increased pulmonary blood flow because of a relevant atrial septal defect (ASD) leads to impaired cardiopulmonary function during maximum exercise in adults. No comparative preoperative and postoperative data are available on the short-term effects of shunt closure on cardiorespiratory function at peak exercise in children. Pulmonary function testing at rest and cardiopulmonary exercise testing together with haemodynamic assessment was done prospectively in children with an ASD preoperatively and again after full recovery at 3-4 mo postoperatively and compared with a matched normal population. Sixteen children, aged 6.8-16.1 y, with a defect of 8-23 mm (median 15 mm) and a pulmonary/systemic flow ratio of 1.5-3.5 (median 2.2) were tested and compared with 15 healthy children. Preoperatively, baseline pulmonary function parameters and exercise capacity were no different from normals. At peak exercise, patients with a shunt had increased pulmonary resistance, especially of the distal airways (p = 0.04), with a significantly larger proportion of children having a paradoxical increase in total airway resistance during exercise (p < 0.05). Maximum serum lactate at peak exercise was elevated (p < 0.05) in patients. In patients, maximum oxygen uptake was impaired (p = 0.03) and remained so at repeat evaluation postoperatively. The same observation was made for chronotropic response to exercise. CONCLUSION: Cardiopulmonary exercise parameters in patients with ASD differed only slightly from those in normal children. The most important deviations were a lower maximum oxygen uptake and an increase in airway resistance at maximum exercise.

Adolescent↗
PubMedDate not supplied

Autonomic nervous function in de novo parkinsonian patients in basal condition and after acute levodopa administration.

The aims of this study were to assess autonomic nervous function in subjects with recently diagnosed Parkinson's disease (de novo patients) and to evaluate its changes following acute levodopa administration. In 13 patients (8 males, 5 females) and 13 age-matched control subjects, three cardiovascular autonomic function tests (Deep Breathing, Valsalva, Lying to Standing) were performed, the QT interval was calculated on a 12-lead electrocardiogram, and the response of plasma norepinephrine to standing was assessed in basal conditions. The cardiovascular tests and the measurement of the QT interval were repeated in de novo Parkinsonian patients 90 minutes after the administration of levodopa 200 mg per os. The results of the Deep Breathing and Valsalva tests were worse and the QT interval longer in patients than in control subjects (although the differences were not statistically significant). The heart rate increase at 30 seconds after standing up was significantly higher in Parkinsonian patients than in the control group. The response of plasma norepinephrine to standing was similar in both groups. Levodopa administration produced a slight improvement in the Deep Breathing test, a shortening of the QT interval and increased tachycardia on standing. Our data suggest that a mild subclinical impairment of parasympathetic function can be a feature of de novo Parkinsonian patients and that levodopa therapy could have a beneficial effect on this autonomic dysfunction.

Adult↗
PubMed1965

Sherpa physiology.

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Acclimatization↗